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Drug: Hydrocortisone
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Total 4 results found since Jan 2013.
Thiram, an inhibitor of 11 ß-hydroxysteroid dehydrogenase type 2, enhances the inhibitory effects of hydrocortisone in the treatment of osteosarcoma through Wnt/β-catenin pathway
CONCLUSIONS: Hydrocortisone inhibits osteosarcoma through the Wnt/β-catenin pathway. Thiram inhibits 11HSD2 enzyme activity, reducing hydrocortisone inactivation and promoting the effect of hydrocortisone through the same pathway.PMID:36978114 | PMC:PMC10045229 | DOI:10.1186/s40360-023-00655-0
Source: BMC Pharmacology and Toxicology - March 28, 2023 Category: Drugs & Pharmacology Authors: You Zhang Nanjing Li He Li Maojia Chen Wei Jiang Wenhao Guo Source Type: research
Vitamin C Prevents Hydrocortisone-Induced Injury in HMEC-1 through Promoting Bestrophin-3 Expression.
CONCLUSIONS: VC can efficiently attenuate HC-induced HMEC-1 cell injury, which may be related to promote Best-3 expression.
PMID: 30672332 [PubMed - as supplied by publisher]
Source: Nutrition and Cancer - January 23, 2019 Category: Cancer & Oncology Authors: Wang X, Zhang G, Zhu C, Lin L, Zhao Z, Yu X, Liu G, Zhang H, Li Q, Dong W, Wang J Tags: Nutr Cancer Source Type: research
Ischemia/reperfusion-induced upregulation of TIGAR in brain is mediated by SP1 and modulated by ROS and hormones involved in glucose metabolism
Publication date: Available online 4 November 2014 Source:Neurochemistry International Author(s): Meiling Sun , Mei Li , Qiao Huang , Feng Han , Jin-hua Gu , Jiaming Xie , Rong Han , Zheng-Hong Qin , Zhipeng Zhou We previously found that TIGAR (TP53-induced glycolysis and apoptosis regulator) was upregulated in response to ischemia/reperfusion insult in a TP53-independent manner. The present study sought to investigate the regulatory mechanisms of TIGAR upregulation in animal and cellular models of stroke. The animal and cellular models of ischemia/reperfusion were produced by transient middle cerebral artery occlusion a...
Source: Neurochemistry International - November 4, 2014 Category: Neuroscience Source Type: research
